Fig. 5.
Fig. 5. Impaired cell cycle progression of DP thymocytes during GVHD. / Acute and chronic GVHD was induced in unirradiated B6D2F1mice. Syngeneically transplanted or naive B6D2F1 mice served as non-GVHD controls. Three developmental stages along the DP→SP differentiation pathway were analyzed at 2 weeks after transplantation for the incorporation of BrdU into cellular DNA. (A) Frequencies (%; mean ± SEM) and (B) absolute cell numbers (×10−3) of cycling cells among DP thymocytes were assessed by flow cytometry of thymocytes from untransplanted (▨) or syngeneically transplanted (□) B6D2F1 mice and from mice with acute (▪) and chronic () GVHD, respectively. The graph represents pooled data from 3 independent experiments; 4 to 7 mice were analyzed for each group. *P < .2 versus mice with chronic GVHD and syngeneic controls, respectively.†P < .02 versus syngeneic controls (ANOVA).

Impaired cell cycle progression of DP thymocytes during GVHD.

Acute and chronic GVHD was induced in unirradiated B6D2F1mice. Syngeneically transplanted or naive B6D2F1 mice served as non-GVHD controls. Three developmental stages along the DP→SP differentiation pathway were analyzed at 2 weeks after transplantation for the incorporation of BrdU into cellular DNA. (A) Frequencies (%; mean ± SEM) and (B) absolute cell numbers (×10−3) of cycling cells among DP thymocytes were assessed by flow cytometry of thymocytes from untransplanted (▨) or syngeneically transplanted (□) B6D2F1 mice and from mice with acute (▪) and chronic () GVHD, respectively. The graph represents pooled data from 3 independent experiments; 4 to 7 mice were analyzed for each group. *P < .2 versus mice with chronic GVHD and syngeneic controls, respectively.P < .02 versus syngeneic controls (ANOVA).

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